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trH3N2 Swine Exposure Exposed
Recombinomics Commentary 14:40
November 19, 2011

• On October 28, 2011, diagnostic testing at the state laboratory was weakly positive for influenza A (H3), but negative for swine-origin influenza targets. The specimen was forwarded to CDC.
• On October 30, 2011, partial genome sequencing confirmed the virus as a swine-origin triple reassortant influenza A (H3N2) virus with the M gene from pH1N1.
• The patient reported multiple instances of close contact with pigs where sick pigs were present.
• No other ill persons have been identified at this time and no human-to-human transmission of this virus is suspected.

The above detail from the CDC report on the two recent trH3N2 clearly illustrates the role of “swine exposure” on testing and detecting trH3N2 cases.  The above case (8M, A/Maine/07/2011) had multiple swine exposures because he attended the Fryeburg fair (which had symptomatic swine), participated in the pig scramble at the fair, and was exposed to asymptomatic swine after the fair.  The Maine CDC used the newly approved PCR test, which can indirectly detect trH3N2 due to cross reactivity of the trH3N2 NP sequence with the H1N1pdm09 NP PCR test.  Thus, trH3N2 can cross react with the seasonal H3 PCR due to the origin of the H3 in swine trH3N2, and can cross react with the H1N1pdm09 NP, and would be negative for the H1N1pdm09 H3 test, which was the profile for the first case from Maine (8M, A/Maine/06/2011).

However, the RNA level in the sample from the second case was low, leading to a weak positive for H3, but a negative for the two swine targets (H3 and NP), which would usually be classified as a seasonal H3N2 case with low levels of RNA.  Since the Maine CDC had just detected a trH3N2 case from a child who had attended the same fair, the sample was sent to the CDC, where partial sequences were generated for HA, NP, MP, NS genes demonstrating that the trH3N2 from the second case in Maine was virtually identical to the first case.

Thus, the second case was identified because of the swine exposure and common exposures at the Fryeburg fair.  However, the two week gap in disease onset dates eliminated the swine at the fair, including the pig scramble as a source for the infection, and the exposure after the fair was to asymptomatic swine.  Thus, although the swine exposure led to testing at the Maine state lab, as well as the CDC, there is no direct evidence (exposure to symptomatic swine with a trH3N2 that matched the two Maine cases).  Moreover, there is also no such evidence for the first case, since the symptomatic swine at the fair tested negative for SOIVs, as indicated in discussions with the Maine department of agriculture.

Similarly, there is no evidence linking the three Pennsylvania cases who attended the Washington County fair, which did not have symptomatic swine.  Only one of the three cases had direct contact with swine (9F, A/Pennsylvania/10/2011), since she was an exhibitor of market hogs, but none of the swine at the fair were symptomatic, including those exhibited by the above case.

Moreover, the first 2011 trH3N2 case (2M, A/Indiana/08/2011) had no swine exposure, but his caretaker did have earlier contact with swine.  However, the caretaker, her family, and associated swine were asymptomatic.  Similary, the most recent Maine case (59M, A/Indiana/10/2011), a veterinarian, had swine contact, but the Indiana BOAH (Board of Animal Health) determined that none of the swine were symptomatic.

Thus, none of the seven confirmed 2011 trH3N2 cases, have been linked to symptomatic swine, other than the first Maine case, but the symptomatic swine at the Fryeburg fair were negative for SOIV.  Thus, the swine “exposure” drives testing at state labs / CDC, which leads to detection of the cases.  No trH3N2 has been identified in any of the swine associated with the seven case, which were all infected with a novel trH3N2 which has the same constellation of genes sharing the same linear.  Matching trH3N2 has not been detected in any swine in the United States, in spite of enhance swine surveillance, and the constellation has also not been tested in swine world wide, including recent trH3N2 with H1N1pdm09 genes isolated from Hong Kong.

Thus, the swine exposure association with trH3N2 case is due to prioritization and sophisticated testing of such cases, which is lacking in cases without swine exposure, where the majority of such cases are not tested beyond a rapid test, which only identifies influenza A positives and does not distinguish between season H3N2, trH3N2, or H1N1pdm09.

The failure to test and sequence these influenza A positive US cases continues to be hazardous to the world’s health.

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